Radio emission of extensive air shower at CODALEMA: Polarization of the radio emission along the v*B vector

Cosmic rays extensive air showers (EAS) are associated with transient radio emission, which could provide an efficient new detection method of high energy cosmic rays, combining a calorimetric measurement with a high duty cycle. The CODALEMA experiment, installed at the Radio Observatory in Nancay, France, is investigating this phenomenon in the 10^17 eV region. One challenging point is the understanding of the radio emission mechanism. A first observation indicating a linear relation between the electric field produced and the cross product of the shower axis with the geomagnetic field direction has been presented (B. Revenu, this conference). We will present here other strong evidences for this linear relationship, and some hints on its physical origin.Comment: Contribution to the 31st International Cosmic Ray Conference, Lodz, Poland, July 2009. 4 pages, 8 figures. v2: Typo fixed, arxiv references adde

Geomagnetic origin of the radio emission from cosmic ray induced air showers observed by CODALEMA

The new setup of the CODALEMA experiment installed at the Radio Observatory in Nancay, France, is described. It includes broadband active dipole antennas and an extended and upgraded particle detector array. The latter gives access to the air shower energy, allowing us to compute the efficiency of the radio array as a function of energy. We also observe a large asymmetry in counting rates between showers coming from the North and the South in spite of the symmetry of the detector. The observed asymmetry can be interpreted as a signature of the geomagnetic origin of the air shower radio emission. A simple linear dependence of the electric field with respect to vxB is used which reproduces the angular dependencies of the number of radio events and their electric polarity.Comment: 9 pages, 15 figures, 1 tabl

Labeling of Multiple HIV-1 Proteins with the Biarsenical-Tetracysteine System

Due to its small size and versatility, the biarsenical-tetracysteine system is an attractive way to label viral proteins for live cell imaging. This study describes the genetic labeling of the human immunodeficiency virus type 1 (HIV-1) structural proteins (matrix, capsid and nucleocapsid), enzymes (protease, reverse transcriptase, RNAse H and integrase) and envelope glycoprotein 120 with a tetracysteine tag in the context of a full-length virus. We measure the impact of these modifications on the natural virus infection and, most importantly, present the first infectious HIV-1 construct containing a fluorescently-labeled nucleocapsid protein. Furthermore, due to the high background levels normally associated with the labeling of tetracysteine-tagged proteins we have also optimized a metabolic labeling system that produces infectious virus containing the natural envelope glycoproteins and specifically labeled tetracysteine-tagged proteins that can easily be detected after virus infection of T-lymphocytes. This approach can be adapted to other viral systems for the visualization of the interplay between virus and host cell during infection

Human Immunodeficiency Virus type 1 Endocytic Trafficking Through Macrophage Bridging Conduits Facilitates Spread of Infection

Bridging conduits (BC) sustain communication and homeostasis between distant tethered cells. These are also exploited commonly for direct cell-to-cell transfer of microbial agents. Conduits efficiently spread infection, effectively, at speeds faster than fluid phase exchange while shielding the microbe against otherwise effective humoral immunity. Our laboratory has sought to uncover the mechanism(s) for these events for human immunodeficiency virus type one (HIV-1) infection. Indeed, in our prior works HIV-1 Env and Gag antigen and fluorescent virus tracking were shown sequestered into endoplasmic reticulum-Golgi organelles but the outcomes for spreading viral infection remained poorly defined. Herein, we show that HIV-1 specifically traffics through endocytic compartments contained within BC and directing such macrophage-to-macrophage viral transfers. Following clathrin-dependent viral entry, HIV-1 constituents bypass degradation by differential sorting from early to Rab11+ recycling endosomes and multivesicular bodies. Virus-containing endocytic viral cargoes propelled by myosin II through BC spread to neighboring uninfected cells. Disruption of endosomal motility with cytochalasin D, nocodasole and blebbistatin diminish intercellular viral spread. These data lead us to propose that HIV-1 hijacks macrophage endocytic and cytoskeletal machineries for high-speed cell-to-cell spread

Molecular Determinants and Dynamics of Hepatitis C Virus Secretion

The current model of hepatitis C virus (HCV) production involves the assembly of virions on or near the surface of lipid droplets, envelopment at the ER in association with components of VLDL synthesis, and egress via the secretory pathway. However, the cellular requirements for and a mechanistic understanding of HCV secretion are incomplete at best. We combined an RNA interference (RNAi) analysis of host factors for infectious HCV secretion with the development of live cell imaging of HCV core trafficking to gain a detailed understanding of HCV egress. RNAi studies identified multiple components of the secretory pathway, including ER to Golgi trafficking, lipid and protein kinases that regulate budding from the trans-Golgi network (TGN), VAMP1 vesicles and adaptor proteins, and the recycling endosome. Our results support a model wherein HCV is infectious upon envelopment at the ER and exits the cell via the secretory pathway. We next constructed infectious HCV with a tetracysteine (TC) tag insertion in core (TC-core) to monitor the dynamics of HCV core trafficking in association with its cellular cofactors. In order to isolate core protein movements associated with infectious HCV secretion, only trafficking events that required the essential HCV assembly factor NS2 were quantified. TC-core traffics to the cell periphery along microtubules and this movement can be inhibited by nocodazole. Sub-populations of TC-core localize to the Golgi and co-traffic with components of the recycling endosome. Silencing of the recycling endosome component Rab11a results in the accumulation of HCV core at the Golgi. The majority of dynamic core traffics in association with apolipoprotein E (ApoE) and VAMP1 vesicles. This study identifies many new host cofactors of HCV egress, while presenting dynamic studies of HCV core trafficking in infected cells

Erratum to: "Nuclear Effects on R=\sigma_L/\sigma_T in Deep-Inelastic Scattering" Phys.Lett. B475(2000)386

This erratum revokes the main conclusion of a Letter that reported measurements of cross sections for deep-inelastic scattering (DIS) of leptons on $^3$He and $^{14}$N targets, expressed as ratios of $\sigma_A / \sigma_D$ to the cross section on the deuterium target.Comment: 3 pages, 1 figur

Radio emission of extensive air shower at CODALEMA: Polarization of the radio emission along the v*B vector

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